Calcium signalling in pancreatic stellate cells: Mechanisms and potential roles

• Ca2+ signals observed in normal pancreatic stellate cells in normal environment.
• Patho-physiologically relevant bradykinin levels elicit Ca2+ signals in stellate cells.
• Bradykinin-evoked Ca2+ signals activate stellate cells.

Hepatic and pancreatic stellate cells may or may not be regarded as stem cells, but they are capable of remarkable transformations. There is less information about stellate cells in the pancreas than in the liver, where they were discovered much earlier and therefore have been studied longer and more intensively than in the pancreas. Most of the work on pancreatic stellate cells has been carried out in studies on cell cultures, but in this review we focus attention on Ca2+ signalling in stellate cells in their real pancreatic environment. We review current knowledge on patho-physiologically relevant Ca2+ signalling events and their underlying mechanisms. We focus on the effects of bradykinin in the initial stages of acute pancreatitis, an often fatal disease in which the pancreas digests itself and its surroundings. Ca2+ signals, elicited in the stellate cells by the action of bradykinin, may have a negative effect on the outcome of the acute disease process and promote the development of chronic pancreatitis. The bradykinin-elicited Ca2+ signals can be inhibited by blockade of type 2 receptors and also by blockade of Ca2+-release activated Ca2+ channels. The potential benefits of such pharmacological inhibition for the treatment of pancreatitis are reviewed.

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